Proceedings of The Physiological Society

University College Dublin (2009) Proc Physiol Soc 15, C48

Oral Communications

Brief sacral nerve root stimulation increases somatosensory cortical activation in the rat.

K. M. Griffin1, C. O’Herlihy2, R. O’Connell3, J. Jones1

1. Physiology, UCD School of Medicine & Medical Science, University College Dublin, Dublin, Ireland. 2. Surgery, Academic Surgical Unit, St Vincent’s University Hospital, ElmPark,, Dublin 4, Ireland. 3. Obstetrics and Gynaecology, National Maternity Hospital, Holles Street,, Dublin 2, United Kingdom.


Faecal incontinence in women is associated with pudendal nerve damage sustained during traumatic childbirth (Snooks et al. 1984). Sacral neuromodulation therapy has been used as a treatment for this condition, but the exact mechanism of action remains unclear. It is possible that affected individuals develop a sensory deprivation syndrome and that sacral neuromodulation increases the sensory input to the cortex. Previous studies carried out by Peirce et al. (2009) showed reduced somatosensory evoked potentials (SEPs) in an animal model of pudendal nerve compression. The aim of this experiment was to study evoked potential following anal canal stimulation before and after acute sacral neuromodulation. Four female virgin Wistar rats (body mass: 200-250g) were anaesthetised with urethane (1.5g/kg i.p.). The femoral artery and vein were cannulated and the animals spontaneously breathed room air supplemented with humidified oxygen. Blood gases and respiration rate were monitored thoughout the experiment. A unilateral craniotomy was performed over the right hemisphere. An extradural recording array (FlexMEA, multi-channel systems: electrode diameter 30µm, electrode spacing 300µm) was placed 2mm lateral and 2mm caudal to bregma. A cathode placed in the anal canal was used to provide triggered stimulation at 1Hz (amplitude: 10volts and pulse duration 0.1ms). A concentric needle electrode was placed in the left S1 sacral foramen (amplitude: 6 volts, frequency 15Hz and duration 1ms). Sixteen cortical evoked potentials were signal averaged (500 sweeps) before and after applying 500sec of sacral neuromodulation. Animals were killed on conclusion of the experiment with an overdose of sodium pentobarbitone (i.v.). The latency to cortical evoked potential was 9.4 ± 0.4 ms and the first positive deflection lasted 131±15 ms. A significant increase was observed in the amplitude of SEP before and after sacral stimulation in all four animals (20.4 ± 7 to 31.8 ± 6 V respectively; P=0.048, one tailed paired Student’s t test). This 50% increase in the amplitude of an evoked potential supports the hypothesis that even brief sacral neuromodulation can increase sensory input to the somatosensory cortex. It remains to be determined if chronic sacral neuromodulation can reverse the blunted SEPs observed in our models of neuropathic faecal incontinence (Peirce et al. 2009).

Where applicable, experiments conform with Society ethical requirements